The relationship between metabolic status and endochondral calcification in the process of bone development following decalcified bone matrix implantation

1992 ◽  
Vol 10 (2) ◽  
pp. 6-10
Author(s):  
Hajime Toba ◽  
Saburou Kakuta ◽  
Tsunahiro Nakamura ◽  
Hidehiko Matsumoto ◽  
Osamu Ohshima ◽  
...  
Keyword(s):  
Bone Development ◽  
Bone Matrix ◽  
Metabolic Status ◽  
The Relationship ◽  
Endochondral Calcification ◽  
Decalcified Bone Matrix

scholarly journals Ostm1 from Mouse to Human: Insights into Osteoclast Maturation

2020 ◽  
Vol 21 (16) ◽  
pp. 5600 ◽  
Author(s):  
Jean Vacher ◽  
Michael Bruccoleri ◽  
Monica Pata
Keyword(s):  
Bone Formation ◽  
Bone Mass ◽  
Bone Fractures ◽  
Bone Development ◽  
Bone Matrix ◽  
Adult Life ◽  
Cell Types ◽  
Severe Form ◽  
Isolation And Characterization

The maintenance of bone mass is a dynamic process that requires a strict balance between bone formation and resorption. Bone formation is controlled by osteoblasts, while osteoclasts are responsible for resorption of the bone matrix. The opposite functions of these cell types have to be tightly regulated not only during normal bone development, but also during adult life, to maintain serum calcium homeostasis and sustain bone integrity to prevent bone fractures. Disruption of the control of bone synthesis or resorption can lead to an over accumulation of bone tissue in osteopetrosis or conversely to a net depletion of the bone mass in osteoporosis. Moreover, high levels of bone resorption with focal bone formation can cause Paget’s disease. Here, we summarize the steps toward isolation and characterization of the osteopetrosis associated trans-membrane protein 1 (Ostm1) gene and protein, essential for proper osteoclast maturation, and responsible when mutated for the most severe form of osteopetrosis in mice and humans.

Decalcified bone matrix increases the osteogenic potential of bone marrow

Bone ◽  
1985 ◽  
Vol 6 (4) ◽  
pp. 280-280
Author(s):  
E. Green ◽  
C. Hinton ◽  
J.T. Triffitt
Keyword(s):  
Bone Marrow ◽  
Bone Matrix ◽  
Osteogenic Potential ◽  
Decalcified Bone Matrix

scholarly journals Body fat distribution and metabolic consequences — Examination opportunities in dogs

2014 ◽  
Vol 62 (2) ◽  
pp. 169-179 ◽  
Author(s):  
Linda Müller ◽  
Eszter Kollár ◽  
Lajos Balogh ◽  
Zita Pöstényi ◽  
Teréz Márián ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Fat ◽  
Regional Distribution ◽  
Subcutaneous Fat ◽  
Metabolic Status ◽  
Metabolic Effects ◽  
Body Regions ◽  
Fat Deposits ◽  
The Relationship ◽  
Fat Volume

The relationship between metabolic disorders and the distribution of fat in different body regions is not clearly understood in humans. The aim of this study was to develop a suitable method for assessing the regional distribution of fat deposits and their metabolic effects in dogs. Twenty-five dogs were subjected to computed tomographic (CT) imaging and blood sampling in order to characterise their metabolic status. The different fat areas were measured on a cross-sectional scan, and the animals’ metabolic status was evaluated by measuring fasting glucose, insulin and leptin levels. The volume of visceral adipose tissue is the main determinant of leptin levels. The correlation of visceral fat volume and leptin concentration was found to be independent of insulin levels or the degree of insulin resistance. There was a positive correlation between the visceral to subcutaneous fat volume ratio and serum insulin concentration, and a similar trend was observed in the relationship of fat ratio and insulin resistance. The distribution of body fat essentially influences the metabolic parameters in dogs, but the effects of adiposity differ between humans and dogs. The findings can facilitate a possible extrapolation of results from animal studies to humans with regard to the metabolic consequences of different obesity types.

scholarly journals The Influences of Casein Phosphopeptides on Metabolism of Ectopic Bone Induced by Decalcified Bone Matrix Implantation in Rats.

1994 ◽  
Vol 40 (2) ◽  
pp. 137-145 ◽  
Author(s):  
Tohru MATSUI ◽  
Hideo YANO ◽  
Takako AWANO ◽  
Tadashi HARUMOTO ◽  
Yasuhiro SAITO
Keyword(s):  
Bone Matrix ◽  
Ectopic Bone ◽  
Casein Phosphopeptides ◽  
Decalcified Bone Matrix

scholarly journals Accumulation, localization, and compartmentation of transforming growth factor beta during endochondral bone development.

1988 ◽  
Vol 107 (5) ◽  
pp. 1969-1975 ◽  
Author(s):  
J L Carrington ◽  
A B Roberts ◽  
K C Flanders ◽  
N S Roche ◽  
A H Reddi
Keyword(s):  
Bone Formation ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Bone Development ◽  
Guanidine Hydrochloride ◽  
Bone Matrix ◽  
Radioreceptor Assay ◽  
Tgf Beta ◽  
Endochondral Bone ◽  
Growth Factor Beta

Endochondral bone formation was induced in postnatal rats by implantation of demineralized rat bone matrix. Corresponding control tissue was generated by implanting inactive extracted bone matrix, which did not induce bone formation. At various times, implants were removed and sequentially extracted with guanidine hydrochloride, and then EDTA and guanidine hydrochloride. Transforming growth factor beta (TGF beta) in the extracts was quantitated by a radioreceptor assay. TGF beta was present in demineralized bone matrix before implantation, and the concentration had decreased by 1 d after implantation. Thereafter, TGF beta was undetectable by radioreceptor assay until day 9. From day 9-21 the TGF beta was extracted only after EDTA demineralization, indicating tight association with the mineralized matrix. During this time, the content of TGF beta per milligram soluble protein rose steadily and remained high through day 21. This increased concentration correlated with the onset of vascularization and calcification of cartilage. TGF beta was detected only between days 3-9 in the controls; i.e., non-bone-forming implants. Immunolocalization of TGF beta in bone-forming implants revealed staining of inflammatory cells at early times, followed later by staining of chondrocytes in calcifying cartilage and staining of osteoblasts. The most intense staining of TGF beta was found in calcified cartilage and mineralized bone matrix, again indicating preferential compartmentalization of TGF beta in the mineral phase. In contrast to the delayed expression of TGF beta protein, northern blot analysis showed TGF beta mRNA in implants throughout the sequence of bone formation. The time-dependent accumulation of TGF beta when cartilage is being replaced by bone in this in vivo model of bone formation suggests that TGF beta may play a role in the regulation of ossification during endochondral bone development.

Effect of glass bioactivity on new bone development induced by demineralized bone matrix in a rat extraskeletal site

1994 ◽  
Vol 113 (4) ◽  
pp. 210-214 ◽  
Author(s):  
K. J. J. Pajam�ki ◽  
�. H. Andersson ◽  
T. S. Lindholm ◽  
K. H. Karlsson ◽  
A. Yli-Urpo ◽  
...  
Keyword(s):  
Bone Development ◽  
Demineralized Bone Matrix ◽  
Bone Matrix ◽  
Demineralized Bone

scholarly journals Skeletal cell YAP and TAZ redundantly promote bone development by regulation of collagen I expression and organization

2017 ◽  
Author(s):  
Christopher D. Kegelman ◽  
Devon E. Mason ◽  
James H. Dawahare ◽  
Genevieve D. Vigil ◽  
Scott S. Howard ◽  
...  
Keyword(s):  
Osteogenesis Imperfecta ◽  
Target Genes ◽  
Bone Development ◽  
Bone Matrix ◽  
Cell Lineage ◽  
Binding Domains ◽  
Conditional Deletion ◽  
Neonatal Lethality ◽  
Allele Dosage

ABSTRACTThe functions of the transcriptional co-activators YAP and TAZ in bone are controversial. Each has been observed to either promote or inhibit osteogenesis in vitro, while their roles in bone development are unknown. Here we report that combinatorial YAP/TAZ deletion from skeletal cells in mice caused osteogenesis imperfecta with severity dependent on targeted cell lineage and allele dosage. Osteocyte-conditional deletion impaired bone accrual and matrix collagen, while allele dosage-dependent deletion from all osteogenic lineage cells caused spontaneous fractures, with neonatal lethality only in dual homozygous knockouts. We identified putative target genes whose mutation in humans causes osteogenesis imperfecta and which contain promoter-proximate binding domains for the YAP/TAZ co-effector, TEAD4. Two candidates, Col1a1 and SerpinH1, exhibited reduced expression upon either YAP/TAZ deletion or YAP/TAZ-TEAD inhibition by verteporfin. Together, these data demonstrate that YAP and TAZ redundantly promote bone matrix development and implicate YAP/TAZ-mediated transcriptional regulation of collagen in osteogenesis imperfecta.

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